Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Measuring NEFA concentrations in insulin resistant and insulin deficient mouse tissue models

ABSTRACT: To compare models of insulin resistance to a model of loss of insulin signaling, we will also determine nonesterified fatty acid metabolites in muscle, using control and streptozotocin (STZ) treated mice as a model of insulin deficient diabetes.

ORGANISM(S): Mouse Mus Musculus

TISSUE(S): Muscle

DISEASE(S): Diabetes

SUBMITTER: Brian O'Neill

PROVIDER: ST000521 | MetabolomicsWorkbench | Wed Dec 07 00:00:00 GMT 2016

REPOSITORIES: MetabolomicsWorkbench

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	mwtab	Other

Items per page:

1 - 1 of 1

Similar Datasets

Measuring ceramide concentrations in insulin resistant and insulin deficient mouse tissue models

Project description:To compare models of insulin resistance to a model of loss of insulin signaling, we will also determine ceramide concentration in muscle, using control and streptozotocin (STZ) treated mice as a model of insulin deficient diabetes.

2016-12-07 | ST000518 | MetabolomicsWorkbench

Measuring TCA cycle concentrations in insulin resistant and insulin deficient mouse tissue models

Project description:To compare models of insulin resistance to a model of loss of insulin signaling, we will also determine TCA cycle metabolites in muscle, using control and streptozotocin (STZ) treated mice as a model of insulin deficient diabetes.

2016-12-07 | ST000520 | MetabolomicsWorkbench

Measuring amino acid metabolites in insulin resistant and insulin deficient mouse tissue models

Project description:To compare models of insulin resistance to a model of loss of insulin signaling, we will also determine amino acid metabolites from muscle, using control and streptozotocin (STZ) treated mice as a model of insulin deficient diabetes.

2016-12-07 | ST000516 | MetabolomicsWorkbench

Measuring acylcarnitine concentrations in insulin resistant and insulin deficient mouse tissue models

Project description:To compare models of insulin resistance to a model of loss of insulin signaling, we will also determine muscle acylcarnitine concentrations, using control and streptozotocin (STZ) treated mice as a model of insulin deficient diabetes. Changes in metabolite profiles will be correlated with activation of mTOR and FoxO pathways in muscle.

2016-12-07 | ST000517 | MetabolomicsWorkbench

Assessing the effect of leptin central administration on plasma proteins in insulin deficient mice.

Project description:Leptin monotherapy (i.e. without the use of administered insulin and/or any other molecule) corrects ID-induced metabolic aberrancies and promotes survival of insulin deficient rodents. These results generated great interest in the possibility of treating insulin deficient patients with leptin and/or molecule(s) underlying its beneficial effects. Hence, with the goal of identifying circulating molecule(s) underlying the advantageous effect of leptin we performed quantitative proteomic analysis of plasma and identified S100A9 as a putative peripheral mediator of leptin action. Here, to identify circulating molecule(s) underlying the advantageous effect of leptin we compared the results obtained by quantitative proteomic analysis of plasma between 2 groups of mice: streptozotocin (STZ)-treated mice that underwent intracerebroventricular (icv) leptin treatment for 12 days (STZ-Leptin) and ii) STZ-treated mice that underwent icv leptin treatment for 10 days and were withdrawn from leptin treatment for the following two days (STZ-Leptin-STOP). STZ treatment led to a massive loss of pancreatic insulin-producing β-cells, diminished pancreatic Proinsulin mRNA level, and caused severe insulinopenia, and hyperglycemia. icv leptin administration normalized hyperglycemia. However, two days after leptin delivery was halted hyperglycemia reappeared. We hypothesized that change in plasmatic protein(s) content could underlie re-emergence of hyperglycemia following decrease of leptin action.

2019-07-12 | PXD013466 | Pride

Bezafibrate improves insulin sensitivity and metabolic flexibility in STZ-treated diabetic mice

Project description:Bezafibrate (BEZ), a pan activator of peroxisome proliferator-activated receptors (PPARs), is generally used to treat hyperlipidemia. Clinical trials on patients suffering from type 2 diabetes indicated that BEZ also has beneficial effects on glucose metabolism, but the underlying mechanisms remain elusive. Much less is known about the function of BEZ in type 1 diabetes. Here, we show that BEZ treatment markedly improves hyperglycemia, glucose and insulin tolerance in streptozotocin (STZ)-treated mice, an insulin-deficient mouse model of type 1 diabetes presenting with very high blood glucose levels. Furthermore, BEZ-treated mice also exhibited improved metabolic flexibility as well as an enhanced mitochondrial mass and function in the liver. Our data demonstrate a beneficial effect of BEZ treatment on STZ mice reducing diabetes and suggest that BEZ ameliorates impaired glucose metabolism possibly via augmented hepatic mitochondrial performance, improved insulin sensitivity and metabolic flexibility. We performed gene expression microarray analysis on liver tissue derived from streptozotocin-treated mice treated with bezafibrate in addition.

2016-06-29 | E-GEOD-79008 | biostudies-arrayexpress

Liver adapts mitochondrial function to insulin-resistant and diabetic states in mice

Project description:Objective: To study if diabetic and insulin-resistant states lead to mitochondrial dysfunction in the liver, or alternatively, if there is adaption of mitochondrial function to these states in the long-term range. Results: High-fat diet (HFD) caused insulin resistance and severe hepatic lipid accumulation, but respiratory chain parameters were unchanged. Livers from insulin-resistant IR/IRS-1+/- mice had normal lipid contents and normal respiratory chain parameters, however showed mitochondrial uncoupling. Livers from severely hyperglycemic and hypoinsulimic, streptozotocin (STZ)-treated mice had massively depleted lipid levels, but respiratory chain abundance was unchanged. However, their mitochondria showed increased abundance and activity of the respiratory chain, which was better coupled compared to controls. Conclusions: Insulin resistance, either induced by obesity or by genetic manipulation, does not cause mitochondrial dysfunction in the liver of mice. However, severe insulin deficiency and high blood glucose levels in mice cause an enhanced performance of the respiratory chain, probably in order to maintain the high energy requirement of the unsuppressed gluconeogenesis. We performed gene expression microarray analysis on liver tissue derived from mice treated with STZ or standard diet (control).

2013-12-10 | E-GEOD-39752 | biostudies-arrayexpress

Transcription profiling of muscle insulin receptor knock-out mice treated with streptozotocin to induce diabetes

Project description:The targeted muscle insulin receptor knockout (MIRKO) model was used, in which there is a complete absence of the insulin-receptor signaling in skeletal muscle but normal insulin and glucose levels. By comparing skeletal muscle gene-expression profiles from MIRKO mice and their controls (lox/lox) under three different metabolic conditions (namely, in the basal state, after streptozotocin (STZ)-induced diabetes, and after STZ-induced diabetes rendered euglycemic with insulin treatment), we can address the following three important questions. (i) What is the direct effect of the loss of insulin signaling on gene expression in skeletal muscle? (ii) What is the contribution of the metabolic and other changes that accompany diabetes to induce indirect changes in gene expression? (iii) How are these pathways regulated and implicated in the pathophysiology of diabetes?

2006-11-24 | E-CBIL-19 | biostudies-arrayexpress

Liver adapts mitochondrial function to insulin-resistant and diabetic states in mice

2013-12-10 | GSE39752 | GEO

Bezafibrate improves insulin sensitivity and metabolic flexibility in STZ-treated diabetic mice

2016-06-29 | GSE79008 | GEO